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| Targets |
Minerval's mechanism of action is multifaceted. It binds to the plasma membrane and alters its lipid organization, which affects the localization and activity of membrane-associated signaling proteins. It is also a fatty acid amide hydrolase (FAAH) inhibitor, which may contribute to its anti-tumor effects by modulating the endocannabinoid system. By disrupting membrane organization, Minerval can affect the function of key signaling pathways involved in cell proliferation and survival, leading to cell cycle arrest and apoptosis. It has been shown to impair cancer cell growth and induce proteolytic cleavage of PARP, a molecular marker of apoptosis.
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| ln Vitro |
(Rac)-Idroxioleic Acid (25-75 μM; 72 hours) inhibits the growth of Jurkat cells in a concentration- and time-dependent manner, with an IC50 of about 40 μM [1]. The molecular marker of apoptosis, PARP, is cleaved by proteases, and (Rac)-idroxioleic acid (25–50 μM; 72 hours) causes a notable, concentration-dependent increase in this process [1].
In vitro, Minerval (25-75 μM) impairs Jurkat cell growth in a time- and concentration-dependent manner, with an IC50 of approximately 40 μM. At concentrations of 25-50 μM over 72 hours, it induces a marked and concentration-dependent increase in the proteolytic cleavage of PARP, a hallmark of apoptosis. These effects are observed in Jurkat cells, a human T-cell leukemia line. The compound's activity is characterized by its ability to disrupt membrane organization and induce apoptotic signaling, making it a valuable tool for studying the role of lipids in cancer cell death. |
| ln Vivo |
In mice in the nude who have been infected with Jurkat cells, (Rac)-idroxioleic acid has been shown to greatly limit tumor growth [1].
In vivo, Minerval significantly inhibits tumor growth in nude mice bearing Jurkat cell xenografts. In a study using 6-week-old nude male mice, oral administration of Minerval at a dose of 600 mg/kg daily for 21 days markedly and significantly inhibited tumor growth. This in vivo efficacy demonstrates the compound's potential as an anti-cancer agent and supports its further investigation. The oral bioavailability of Minerval is a key factor for its in vivo activity. |
| Enzyme Assay |
In vitro enzyme/receptor binding studies for Minerval are not typical, as its mechanism involves membrane interaction and enzyme inhibition. Its activity as a fatty acid amide hydrolase (FAAH) inhibitor can be assessed using enzyme activity assays. In these assays, recombinant FAAH is incubated with a substrate in the presence of varying concentrations of Minerval, and the inhibition of substrate hydrolysis is measured. These studies would help to characterize its potency as a FAAH inhibitor. However, its primary anti-tumor mechanism is thought to be related to its effects on membrane organization rather than FAAH inhibition.
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| Cell Assay |
Cell Viability Assay[1]
Cell Types: Jurkat cells Tested Concentrations: 25 μM, 50 μM, 75 μM Incubation Duration: 24 hrs (hours), 48 hrs (hours), 72 hrs (hours) Experimental Results: Jurkat cell growth is affected in a time- and concentration-dependent manner. Western Blot Analysis [1] Cell Types: Jurkat cells Tested Concentrations: 25 μM, 50 μM Incubation Duration: 72 hrs (hours) Experimental Results: Induced PARP proteolytic cleavage Dramatically and concentration-dependently increased. In vitro cellular assays for Minerval are used to study its effects on cancer cells. In these experiments, cancer cell lines, such as Jurkat cells, are treated with the compound. Cell viability is assessed using standard assays like MTT or CellTiter-Glo to determine the IC50. Apoptosis is evaluated by measuring the proteolytic cleavage of PARP using Western blotting. Cell cycle analysis by flow cytometry can also be performed to determine the phase of cell cycle arrest. These assays confirm the compound's mechanism of action and its potential as an anti-cancer agent. |
| Animal Protocol |
Animal/Disease Models: 6weeks old male nude mice (Jurkat cell xenograft model) [1]
Doses: 600 mg/kg Route of Administration: Oral; daily; 21 days Experimental Results: Dramatically inhibited tumor growth. In vivo animal studies for Minerval are conducted in xenograft mouse models. In one study, nude mice were implanted with Jurkat cells, and then treated with Minerval. The compound was administered orally at 600 mg/kg daily for 21 days. The primary endpoint was tumor growth inhibition, which was markedly and significantly reduced in the treated group compared to controls. These studies are essential for demonstrating the compound's in vivo efficacy and for supporting its potential as a therapeutic agent. |
| ADME/Pharmacokinetics |
Pharmacokinetic properties of Minerval include its molecular weight of 298.46 g/mol and a molecular formula of C18H34O3. It is a small, lipophilic molecule, which is typical for fatty acid derivatives. Its chemical name is (9Z)-2-hydroxyoctadec-9-enoic acid. It is soluble in DMSO at 100 mg/mL. Its oral bioavailability is suggested by its efficacy in animal studies when administered orally. However, specific data on its half-life, metabolism, and excretion are not detailed in the provided sources.
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| Toxicity/Toxicokinetics |
Toxicological data for Minerval are limited, as it is a research compound. Its primary value is as a tool for studying lipid biology and cancer. While specific toxicity profiles are not detailed, its mechanism of altering membrane organization and inhibiting FAAH could have significant physiological effects. Comprehensive safety studies would be required for its development as a therapeutic agent. As with all research chemicals, it should be handled with appropriate laboratory safety precautions.
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| References |
[1]. Llado V, et al. Minerval induces apoptosis in Jurkat and other cancer cells. J Cell Mol Med. 2010 Mar;14(3):659-70.
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| Additional Infomation |
2-Hydroxyoleic acid (2-hydroxyoleic acid) is a 2-hydroxy fatty acid formed by introducing a hydroxyl group at the 2-position of oleic acid. It is a highly bioavailable synthetic hydroxylated fatty acid that can regulate lipid content in cancer cell membranes and induce cell cycle arrest and apoptosis in various cancer cell lines. It possesses antitumor, apoptosis-inducing, and hypotensive effects. It is a 2-hydroxy fatty acid, a long-chain fatty acid, and a hydroxy monounsaturated fatty acid, functionally related to oleic acid, and is the conjugate acid of 2-hydroxyoleic acid esters. Adrolol oleic acid (ADO) is a highly bioavailable synthetic oleic acid analog with potential antitumor activity. After administration, ADO activates sphingomyelin synthase (SMS), thereby increasing the concentration of sphingomyelin (SM) and diacylglycerol (DAG) in tumor cell membranes and decreasing the levels of phosphatidylethanolamine (PE) and phosphatidylcholine (PC) in the membrane. This restores the normal levels and proportions of membrane lipids. By restoring normal membrane lipid structure and composition, this drug inhibits membrane protein-related signaling and the activity of abnormal signaling pathways in certain tumor cells, including the Ras/MAPK and PI3K/AKT pathways. This inhibits tumor cell proliferation, induces tumor cell differentiation, and ultimately leads to cell death.
Minerval is a research-use-only compound that acts as a fatty acid amide hydrolase inhibitor and an anti-tumor agent. Its CAS number is 56472-29-8. It is also known as 2-Hydroxyoleic acid, 2-OHOA, and (Rac)-Idroxioleic acid. By binding to the plasma membrane and altering lipid organization, it induces cell cycle arrest and apoptosis in cancer cells. It has shown efficacy in mouse xenograft models. It is not an approved drug and is intended for non-clinical research applications. |
| Molecular Formula |
C18H34O3
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|---|---|
| Molecular Weight |
298.46
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| Exact Mass |
298.251
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| CAS # |
56472-29-8
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| PubChem CID |
9796304
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| Appearance |
Typically exists as solid at room temperature
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| LogP |
5.079
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| Hydrogen Bond Donor Count |
2
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| Hydrogen Bond Acceptor Count |
3
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| Rotatable Bond Count |
15
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| Heavy Atom Count |
21
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| Complexity |
261
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| Defined Atom Stereocenter Count |
0
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| SMILES |
CCCCCCCC/C=C\CCCCCCC(C(=O)O)O
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| InChi Key |
JBSOOFITVPOOSY-KTKRTIGZSA-N
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| InChi Code |
InChI=1S/C18H34O3/c1-2-3-4-5-6-7-8-9-10-11-12-13-14-15-16-17(19)18(20)21/h9-10,17,19H,2-8,11-16H2,1H3,(H,20,21)/b10-9-
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| Chemical Name |
(Z)-2-hydroxyoctadec-9-enoic acid
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| Synonyms |
2 OHOA; 2OHOA; 2-OHOA
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: This product requires protection from light (avoid light exposure) during transportation and storage. |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
DMSO : ~100 mg/mL (~335.05 mM)
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| Solubility (In Vivo) |
Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.
Injection Formulations
Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution. Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline) Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil) Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals). View More
Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)] Oral Formulations
Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium) Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals). View More
Oral Formulation 3: Dissolved in PEG400 (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 3.3505 mL | 16.7527 mL | 33.5053 mL | |
| 5 mM | 0.6701 mL | 3.3505 mL | 6.7011 mL | |
| 10 mM | 0.3351 mL | 1.6753 mL | 3.3505 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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